Tumors undergo metabolic reprogramming to support the synthesis of new macromolecules required for rapid cell division, additionally providing a selective advantage for progression and protection from death (Cairns et al., (2011) Nature Revs. Cancer 11: 85-95). The concept of metabolic adaptation in tumors was first described by Otto Warburg in the 1920s following the discovery that cancer cells display increased rates of glucose utilization in comparison to normal tissue, even under aerobic conditions (Warburg O. (1956) Science 123: 309-314). It is now known that the metabolic transformation of cancer cells encompasses multiple interconnecting metabolic networks (Carracedo et al., (2013) Nature Revs. Cancer 13: 227-232), with feedback loops and crosstalk acting to provide plasticity for cells to survive the steep and localized nutrient and oxygen gradients in the harsh tumor microenvironment (Gatenby & Gillies (2004) Nature Revs. Cancer 4: 891-899). Central to tumor metabolism is the glycolytic pathway that sustains tumors by generating ATP and by synthesizing intermediates for biosynthetic pathways.